The topic of gas emboli is miscellaneous enough to be fitted into the "misc" section of SAQs. The most likely causes include surgical mishaps, particularly cardiothoracic (and so it could have easily slotted into the cardiothoracic ICU section). If discussion were limited to cerebral arterial gas embolism, it could be classified as a predominantly neurological issue and parked in the neurology/neurosurgery section. These would be logical options. However the author of Deranged Physiology is unencumbered by logic, and had instead opted to put gas emboli into the Trauma/ Drowning section, as by far the most interesting cause of such emboli is decompression injury, and because it allows him to digress extensively on the topic of exposing humans to pressurised gas.
This has only ever come up once in the exams, in Question 21 from the first paper of 2017. Specifically, the college wanted to hear about the trials and tribulations of transporting a patient with a cerebral arterial gas embolism - how the specific pathology affects aeromedical retrieval, for example. With any luck, this topic (like traumatic asphyxia and resuscitative thoracotomy) will be the subject of a once-off "everybody fails" question, never appearing again in the exams. One questions the role of examining such esoterica. Did this question really discriminate safe competent intensivists from unsafe ones?
Whinge aside, let us explore the literature references. The most often cited article for this topic is the NEJM paper by Muth and Shank (2000), available for free through dive-shield.us. It is unclear whether these guys are aware that they are hosting it. For a detailed discussion of venous gas emboli, the single best resource is probably Palmon et al (1997). To answer Question 21 with a question-specific article, one would use Jeffrey Stephenson's 2009 paper, "Pathophysiology, treatment and aeromedical retrieval of SCUBA-related DCI"
In brief summary:
Clinical features of gas embolism:
- PEA arrest
- "mill wheel" murmur
- Gas bubbles in the retina (on ophthalmoscopy)
- Drop in EtCO2
- ECG features of right heart strain
- Pulmonary hypertension
Management of gas embolism:
- Avoid giving N2O
- Increase FiO2 to 100%
- Put the patient in supine position
- Try to aspirate the gas from the RV using a long catheter, eg. a 25cm CVC
- Hyperbaric oxygen therapy is indicated
- Antiepileptic therapy is indicated if the patient has a cerebral gas embolism
Without further ado, here are the major reasons for gas emboli.
Mixed (i.e. possibility of both arteral and venous)
In order for gas to make its way into your circulatory system, several things need to go wrong in a major way. Usually, there needs to be a breach in the circulatory system (a wound, a vascular access device, etc) and the blood in this open vessel needs to be under lower pressure than the available gas. If not for the latter clause, all minor paper cuts would give rise to air emboli. These preconditions mean that venous emboli are by far more likely (as a part of the upper body venous circulation is constantly under negative pressure) and that any invasive procedure involving insufflation poses a potential risk (and this includes positive pressure ventilation). The more rare (and interesting) scenario is one where abrupt ambient pressure changes affect the solubility of dissolved gases in the body fluids, causing them to emerge out of solution in the form of bubbles. A possible third option is isobaric counterdiffusion, where gases with different blood solubility compete for limited "space" within the liquid phase, the more soluble gas forcing the less soluble one out of solution. This is generally limited to the skin and middle ear, and (though painful and crippling) is rarely a reason for ICU admission.
How much air do you need to kill somebody? Basically, you need to fill the right ventricular outflow tract with gas to cause a cardiac arrest (it usually looks like PEA with tachycardia). Oppenheimer et al (1953) observed this phenomenon in dogs, and found that 7.5ml/kg was the LD100 (i.e. every dog died). In contrast, slow infusion of gas seems relatively benign; Hybels (1980) reports that up to 1400ml of gas is reasonably well tolerated in dogs, provided it happens over several hours.
What about humans? Palmon et al (1997) give a good rundown of these events, and offers a bibliography of case reports. For instance, Allen Yeakel (1968) reports on a lethal venous air embolism of approximately 136ml, which was administered accidentally during an exchange of a plastic blood storage container (the patient was undergoing a carotid endarterectomy). Harrison Martland in 1945 wrote an article describing fatal air emboli in patients who used "powder insufflators" to squirt air into their vaginas for the purpose of antitrichomonal treatment, a technique which is thankfully no longer a part of the gynaecological repertoire because the risk of air embolism is now well-appreciated. That has not stopped people from insufflating each other's vaginas recreationally, with fatal consequences. Judging by the number of case reports this is actually suprisingly commonplace, which somewhat redefines the term "high-risk sexual activity". Less hideous case reports are also available where emboli are the consequence of lung biopsy, bronchogenic cyst rupture, gastrointestinal endoscopy and arthroscopy. Given that it is hard to estimate the volume of air postmortem, Palmon et al conclude that the sudden injection of about 100-300ml of air is enough to cause circulatory arrest.
Is this relevant? The CICM exam has only ever approached this issue once, in Question 18 from the second paper of 2019 where gas embolism is only one potential differential in the cardiac arrest of a patient who is equally likely to be aspirating or having a PE. The college focused on clinical features and management, which is the subject of the following paragraphs.
Obviously, the exact pathophysiological features of gas embolism depend heavily upon where precisely the embolism went. In the case of the cerebral gas embolism in Question 21 from the first paper of 2017, the college wanted to hear about the trials and tribulations of transporting a patient with a cerebral arterial gas embolism. The following discussion is of the generic clinical consequences of a venous gas embolism, ranging from symptoms and signs to TTE findings and PA catheter measurements.
The following strategies are anaesthetic-sounding because they were written by an anaesthetist to help manage a complication during anaesthesia. However, they are worth knowing about for the ICU environment.
This finally answers Question 21 from the first paper of 2017, in which a cerebrally embolised SCUBA diver is waiting for you to organise their retrieval to the nearby hyperbaric chamber (300km away).